Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The report is based on a four-centre study on 25 patients with coronary insufficiency (ECG signs). In random sequence the following were given to each patient: a nitrate (isosorbide dinitrate), carbocromene, practolol, and oxyphedrine. The initial criterion for inclusion was S-T depression of 0.2 mV on stepwise exercise (bicycle ergometry). S-T depression, systolic blood pressure and heart rate changes were used as criteria. For each drug there was an acute test and a long-term test of 12 days. The Friedman test was used for the statistical evaluation of the results. Isosorbide dinitrate decreased the extent of S-T depression in the acute tests while practolol did so in the long-term test. Practolol reduced systolic pressure on long-term administration, with no difference in the acute experiment. Heart rate was reduced by practolol both acutely and long-term. These results give no indication for any possible differential treatment of coronary insufficiency, but this may be due to the selection of patients in this study.
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PMID:[Clinical studies on the effect of drugs used in the treatment of angina]. 108 22

Significant reduction of angina threshold (145 Imp./min to 134 Imp./min) and increase of ST-segment depression (0.13 to 0.17 mV) indicating progression of coronary artery disease was seen in 34 subjects studied by atrial pacing at intervals betion (0.22 mV to 0.12 mV) during exercise, which correlated significantly with decrease of heart rate (121 to 110 beats/min), is interpreted as consequence of diminished sympathetic activity and myocardial O(2)-demand. The change of hemodynamic parameters during controlled exercise does not allow evaluation concerning the progress of coronary artery disease, whereas cardiac stress test with atrial pacing is reproducible. There was no difference in relation to reduction of angina threshold between the group after combined longterm medication with nitrate and ss-blocking agent and the control group. Plasma lipid abnormalities were predictive of subsequent reduction of angina threshold. Severe 2 and 3 vessel obstruction was seen more frequently in patients exhibiting reduction of angina threshold. Level of uric acid, obesity, hypertension, age, combination of risk factors, the initially studied myocardial lactate production and angina threshold during exercise and atrial pacing had no predictive value concerning reduction of angina threshold.
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PMID:[Course of coronary disease. Evaluation of prognosis and progression of coronary insufficiency with atrial pacing and ergometry]. 113 Jan 29

Studies were conducted to determine the effects of high levels of dietary silver nitrate and copper sulfate on the response of chicks to toxic levels of dietary selenium. Adding 5 ppm or more selenium to a basal stock diet significantly reduced growth rate, and 40 ppm or high significantly increased mortality during the 2-week experiments. Deitary silver or copper (1,000 ppm) counteracted the growth depression and prevented mortality at the higher levels of selenium. Hepatic selenium reached a maxiumum in chicks fed the basal diet with 10 ppm dietary selenium. Hepatic selenium of chicks fed silver was less than that of the control chicks when diets containing 10 ppm or less selenium were fed. Adding copper to the diet resulted in considerable accumulation of selenium in the liver, which was evident even at the lower levels of added selenium. Rseults of an experiment to determine the effects of deitray silver and copper on the distribution of 75-Se administered either orally or in tramusculary showed that silver interfered with absorption of selenium. The results of these experiments suggest that silver modifies selenium toxity both by interfering with selenium absorption and by causing the accumulation of a nondeleterious selenium compound in the tissues. Copper modifies selenium toxicity primarily by causing the accumulation of a nondeleterious compound in the tissues.
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PMID:Modification of a selenium toxicity in chicks by dietary silver and copper. 114 4

In experiments with rabbits, glucagon prolonged the half-period of absorption of sodium iodide 125J in the left ventricular myocardium. Regitine prevented acceleration of the heart rate and impairment of capillary flow after glucagon. In healthy rabbits hippurate 125J clearance was unaffected by glucagon. After injury of the heart muscle by injection of silver nitrate solution into the left ventricular wall and depression of blood pressure, glucagon partly normalized renal clearance of hippurate 125J.
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PMID:The influence of glucagon on the blood supply of the heart and kidneys in rabbits. 121 13

The purpose of the two double-blind studies summarized in this article was to compare the antianginal and anti-ischemic effects of nicorandil with those of two different nitrate preparations. A total of 129 patients with stable New York Heart Association functional class II or III coronary heart disease were enrolled in the studies. Ninety-five patients received nicorandil, 34 received isosorbide dinitrate (ISDN), and 63 received isosorbide-5-mononitrate (MN). In study 1, nicorandil was compared with MN in a crossover design with 54 protocols eligible for efficacy assessment of MN and 52 eligible for nicorandil, respectively. Twenty milligrams of nicorandil and 20 mg MN administered b.i.d. for 4 weeks were equally effective in the treatment of stress-induced angina. Both drugs prolonged bicycle exercise tolerance and reduced weekly anginal attack rates. In study 2, nicorandil and ISDN were administered to two parallel groups of patients at a dose of 10 mg t.i.d. for 2 weeks and then 20 mg t.i.d. for 4 weeks. Under the assumption that the repetitive administration of nitrates with short dosing intervals might induce the development of tolerance to the nitrate mechanism of action, the t.i.d.-dosing regimen had been chosen in this study. Thirty-two protocols from those receiving nicorandil and 34 protocols from those receiving ISDN were eligible for efficacy assessment. Both drugs increased exercise capacity and reduced ST-segment depression at identical work loads with no significant difference between groups (p > 0.05). For both drugs, the higher doses were more effective than the lower doses. tolerance to the nitrate mechanism of action did not develop with either drug.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antianginal and anti-ischemic efficacy of nicorandil in comparison with isosorbide-5-mononitrate and isosorbide dinitrate: results from two multicenter, double-blind, randomized studies with stable coronary heart disease patients. 128 80

The efficacy of sustained-release (s.r.) verapamil and conventional verapamil were compared in a double blind, crossover study in 20 patients (age 53 +/- SD6 years) who had stable effort angina and had used betablockers and long acting nitrates for at least two weeks. All patients received s.r. verapamil 200 mg b.i.d. and conventional verapamil 120 mg t.i.d. in a randomised order for two weeks. A symptom limited bicycle exercise test was performed at the end of the patients' previous medication period with betablocker plus long acting nitrate and at the end of both verapamil treatments in the morning before drug administration and three hours thereafter. All the patients improved subjectively during both verapamil regimens according to NYHA classification and they had fewer anginal attacks. The time to onset of ST-segment depression during exercise remained shorter during beta-blockade and long acting nitrates than during both verapamil regimens (P less than 0.05). During the peak action three hours after drug administration conventional verapamil was most effective at comparable workloads (P less than 0.05), whereas the exercise time was slightly prolonged with s.r. verapamil before drug administration.
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PMID:Efficacy of conventional and sustained-release verapamil in stable angina pectoris. 134 86

1. We have investigated whether the myocardium and isolated cardiac myocytes can express a Ca(2+)-independent NO synthase after treatment with endotoxin or cytokines. Nitric oxide synthesis was measured in cytosols from the left ventricular wall from rats treated with endotoxin, or from freshly isolated myocytes from adult rats treated in vitro with cytokines. 2. Cytosols from the ventricle of saline-treated control animals showed only Ca(2+)-dependent NO synthesis. After treatment with endotoxin, the expression of an inducible, Ca(2+)-independent NO synthase was observed. The activity of this enzyme was maximal at 6 h and returned towards control levels by 18 h; no alterations occurred in the Ca(2+)-dependent NO synthase activity. Parallel to this enzyme induction there was an increase in myocardial guanosine 3':5'-cyclic monophosphate (cyclic GMP) and plasma nitrite and nitrate (NOx-). All these changes were prevented by pretreatment of the rats with dexamethasone. 3. Myocytes possessed Ca(2+)-dependent NO synthase activity and expressed, after treatment with tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta), a Ca(2+)-independent NO synthase, the induction of which was prevented by dexamethasone and cycloheximide. 4. Since increases in cyclic GMP levels in the heart are associated with reduced myocardial contractility, it is possible that the enhanced production of NO by a Ca(2+)-independent enzyme accounts, at least in part, for the depression of myocardial contractility seen in septic shock, cardiomyopathies, allograft rejection, burn trauma, as well as during anti-tumour therapy with cytokines.
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PMID:Induction and potential biological relevance of a Ca(2+)-independent nitric oxide synthase in the myocardium. 137 38

Nitrate monotherapy was assessed by treadmill exercise stress testing in 18 patients with significant but relatively asymptomatic myocardial ischemia who were receiving no other antianginal therapy. In addition, prolonged ambulatory electrocardiographic monitoring was performed in 7 patients with demonstrable ischemia during baseline monitoring. After baseline assessment, 5 treatment periods were used in a random order (each of 1 week duration), incorporating 2 dose levels of transdermal nitrate (10 and 20 mg/24 hours) and isosorbide dinitrate (ISDN) (30 and 60 mg/day in divided doses) with a 10-hour nitrate-free interval every 24 hours, as well as a placebo period using a double-blind technique. All treatment periods (including placebo) showed a significant (p < 0.01) 45 to 69% prolongation in the time to 1 mm ST depression during exercise. Paired baseline times of 231 +/- 28 and 233 +/- 30 seconds increased to 367 +/- 37 seconds with 30 mg/day of ISDN, 393 +/- 37 seconds with 60 mg/day of ISDN, 381 +/- 31 seconds with 10 mg/day of transdermal nitrate, and 372 +/- 33 seconds with 20 mg/day of transdermal nitrate. The value for placebo was 342 +/- 29 seconds, which was not significantly different from active treatment (p > 0.1). Some patients appeared to individually respond to > or = 1 nitrate preparation significantly more than to placebo, but this appeared to be unpredictable and largely independent of dosage level and route of administration. There was a qualitatively similar but statistically insignificant reduction in total ischemic time during ambulatory monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Placebo effect of nitrate monotherapy for myocardial ischemia. 144 72

The tone of vascular smooth muscle is influenced by factors released from the endothelium, including endothelin (ET)-1 and endothelium-derived relaxing factor (EDRF). To better understand the interactions between these two mediators, we examined the release of both immunoreactive ET-1 (ir-ET-1) and EDRF from bovine aortic intact endothelium. Bovine aortas were opened longitudinally, washed, and clamped with the endothelium uppermost between two plates. The upper plate contained six openings forming identical and independent wells of endothelial cell monolayer. In experiments examining the release of EDRF, measured as accumulated NO2- and NO3- (NO chi -), we found that ET-3, calcium ionophore A23187 (A23187), acetylcholine (ACh), or ADP caused significant increase in NO chi- release, whereas ET-1 did not. These were significantly reduced in the presence of the EDRF/NO synthase inhibitor, NG-methyl-L-arginine (L-NMA). In a parallel series of experiments measuring EDRF release by stimulation of guanosine 3',5'-cyclic monophosphate (cGMP) accumulation in rat fetal lung (RFL)-6 cells, ET-3 but not ET-1 was also found to be active as a releaser of EDRF. A23187 caused an increase of ir-ET-1 release, whereas ACh, ADP, or the NO-containing compound sodium nitroprusside decreased the release of ir-ET-1. The depression in ir-ET-1 release in the presence of ACh or ADP was not seen when the endothelium was treated with L-NMA. When the cells were pretreated with 8-bromoguanosine 3',5'-cyclic monophosphate (8-bromo-cGMP), the release of ir-ET-1 in response to A23187 was significantly depressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interactions of endothelins and EDRF in bovine native endothelial cells: selective effects of endothelin-3. 159 Apr 65

The magnitude of tolerance to the anti-anginal efficacy of transdermal nitroglycerin and the efficacy and safety of short (4 h) and long (10 h) nitrate-free intervals for its prevention, were investigated in a randomized, double-blind, placebo-controlled crossover trial of 4 week-long treatment regimens: placebo, continuous therapy with a 50 mg patch (10 mg.24 h-1), and 4 h and 10 h nitrate-free periods. Only patients showing greater than 1 min increase in time to 1 mm ST depression after acute patch administration were eligible. Twelve men completed the study. One other anti-anginal medication (a beta-blocker in nine and calcium antagonist in two) was permitted in a constant dose throughout the study. Patients underwent exercise testing on days 1 and 7 of each treatment period, and 24 h ambulatory ECG monitoring on day 6. Compared to placebo, transdermal nitroglycerin on day 1 significantly improved time to 1 mm ST depression by 35%, and time to angina, exercise duration and maximal workload by 21%, 13% and 9% respectively. These improvements were totally lost after 7 days' continuous therapy, but completely maintained by a 10 h nitrate-free period (improvements of 35%, 25%, 16% and 11% respectively) but not by a 4 h nitrate-free period (non-significant improvements of 15%, 2%, 4% and 1% respectively). The differences between 10 and 4 h nitrate-free were significant for each end-point. Neither duration of ambulatory ischaemia, nor the proportion of patients experiencing greater than or equal to 5 min ischaemia during the scheduled nitrate-free interval differed between treatments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy, safety and duration of nitrate-free interval to prevent tolerance to transdermal nitroglycerin in effort angina. 161 12


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